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Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville, Virginia 22908; and The Lutcher Brown Department of Biochemistry, The Whittier Institute for Diabetes and Endocrinology LaJolla, California 92037
Address requests for reprints to: Dr. M. O. Thorner, Department of Internal Medicine, University of Virginia School of Medicine, Box 511, Charlottesville, Virginia 22908.
Abstract
The hemolytic plaque assay technique can be used to detect specific hormone release from single pituitary cells. Using antisera raised against murine GH or rat PRL, we have enumerated the active lactotropes and somatotropes from male and female rat pituitary glands. These studies reveal sexrelated differences in the number of cells exporting GH and PRL among anterior pituitary cells in culture. In the presence of human GH-releasing factor (hGRF), the mean percentage of GH cells was 53% in males and 30% in females (P < 0.005). The mean percentage of PRL cells was 15% in males and 39% in females (P < 0.008). These values were not significantly altered when hGRF was omitted. The sum of GH and PRL cells identified in separate plaque assays significantly exceeds the number obtained when GH and PRL cells were determined concurrently with a simultaneous plaque assay for both hormones. This difference is dependent on the presence of hGRF, since there was no difference when hGRF was omitted. These data identify the mammosomatotrope in numbers lower than previous reports. By this approach, the mammosomatotrope subpopulation numbers about 5% of all cells in culture. In summary, we demonstrate a sex-related difference in the number of cells exporting GH or PRL among pituitary cells in culture. This difference corresponds with and may underly sex-related differences in the responsiveness of GH and PRL secretion from the pituitary gland. Furthermore, a minor subpopulation of normal pituitary cells appears capable of simultaneous secretion of both GH and PRL. (Endocrinology 116: 1371-1378, 1985)
Footnotes
* This work was supported by NIH Research Grants AM-32632 and HD-13197 (to M.O.T.).
Received June 27, 1984.
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